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Chronic and acute regulation of intestinal triglyceride metabolism genes by dietary fat.

机译:膳食脂肪对肠道甘油三酸酯代谢基因的慢性和急性调节。

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摘要

Excess dietary fat is associated with obesity and metabolic syndrome. The small intestine efficiently absorbs a range of dietary triglyceride, suggesting intestinal adaptation to various triglyceride intakes. In the current study, we analyze intestinal mRNA levels of proteins involved in intestinal triglyceride metabolism in lean and diet induced obese mice. Obese mice show increased intestinal adipose differentiation related protein, peroxisome proliferator-activated receptor alpha, peroxisome proliferator-activated receptor gamma, acyl-CoA oxidase, diacylglycerol acyltransferase 2, apolipoprotein A-IV, fatty acid transporter and liver fatty acid binding protein mRNA levels. We also analyzed mRNA levels of proteins involved in intestinal triglyceride metabolism in lean and diet induced obese mice in response to a high fat challenge. Lean mice have increased tail interacting protein of 47 kDa, adipose differentiation related protein, adipose triglyceride lipase, comparative gene identification 58, diacylglycerol acyltransferase 2, microsomal triglyceride transfer protein and fatty acid transporter mRNA levels post bolus. Conversely, diet induced obese mice do not have increased mRNA levels post bolus and lipolytic enzyme mRNA levels are decreased. Lipid droplet associated protein levels also dynamically increase and later decrease post bolus in lean mice. Increased lipid droplet associated protein levels are blunted in diet induced obese mice. Overall, the small intestinal mucosa adapts to both diet induced obesity and a high fat challenge in lean and diet induced obese mice.
机译:膳食脂肪过多与肥胖和代谢综合症有关。小肠可有效吸收一系列饮食中的甘油三酸酯,表明肠道对各种甘油三酸酯摄入量都有适应性。在当前的研究中,我们分析了肥胖和饮食诱发的肥胖小鼠肠道甘油三酸酯代谢中蛋白质的肠道mRNA水平。肥胖小鼠的肠道脂肪分化相关蛋白,过氧化物酶体增殖物激活的受体α,过氧化物酶体增殖物激活的受体γ,酰基辅酶A氧化酶,二酰基甘油酰基转移酶2,载脂蛋白A-IV,脂肪酸转运蛋白和肝脏脂肪酸结合蛋白mRNA水平升高。我们还分析了在肥胖和饮食诱导的肥胖小鼠对高脂挑战的反应中,肠道甘油三酸酯代谢中涉及的蛋白质的mRNA水平。瘦小鼠的尾部相互作用蛋白增加了47 kDa,脂肪分化相关蛋白,脂肪甘油三酸酯脂肪酶,比较基因鉴定58,二酰基甘油酰基转移酶2,微粒体甘油三酸酯转移蛋白和大剂量后脂肪酸转运蛋白mRNA水平。相反地​​,饮食诱导的肥胖小鼠在推注后不具有增加的mRNA水平,而脂解酶mRNA的水平降低。在瘦小鼠中,脂质滴相关的蛋白质水平也会在推注后动态增加,随后降低。在饮食诱导的肥胖小鼠中,与脂质滴相关的蛋白质水平增加而变得迟钝。总体而言,小肠粘膜既可以适应饮食诱发的肥胖,也可以适应肥胖和饮食诱发的肥胖小鼠的高脂挑战。

著录项

  • 作者

    Rosen, Mary C. W.;

  • 作者单位

    Purdue University.;

  • 授予单位 Purdue University.;
  • 学科 Nutrition.
  • 学位 M.S.
  • 年度 2011
  • 页码 117 p.
  • 总页数 117
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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